Tooth caries are the result of a dietary carbohydrate-modified bacterial infectious disease, one of the most common bacterial infections in humans (Loesche, 1986; van Houte, 1994; Featherstone, 2000). The basic mechanism of dental caries is demineralization, or mineral loss, through attack by acid generated by bacteria (Featherstone, 2004; Deng, 2005; Totiam et al., 2007). Therefore, acidogenic bacteria growth, typically in the context of plaque and biofilm formation, is responsible for dental caries (Loesche, 1986; van Houte, 1994; Zero, 1995; Featherstone, 2000; Deng et al., 2005; Cenci et al., 2009). Plaque formation has been described to have three steps: pellicle formation, bacteria colonization, and biofilm maturation (Burne, 1998). In the initial stage, a proteinaceous film called pellicle forms on the tooth surface with adsorbed components from saliva, mucosa, and bacteria (Carlen et al., 2001). Bacteria then adhere and colonize on this surface to grow into a biofilm, which is a heterogeneous structure consisting of clusters of various types of bacteria embedded in an extracellular matrix (Stoodley et al., 2008). Cariogenic bacteria such as Streptococcus mutans (S. mutans) and lactobacilli in the plaque can take nutrients from carbohydrates and produce organic acids. Acid production causes demineralization to the tooth structure beneath the biofilm.
Resin composites have been increasingly used for tooth cavity restorations because of their aesthetics, direct-filling capability, and enhanced performance (Ferracane, 1995; Bayne et al., 1998; Lim et al., 2002; Ruddell et al., 2002; Watts et al., 2003; Drummond, 2008). While there has been significant improvement in resin compositions, filler types, and cure conditions since their introduction (Ruddell et al., 2002; Imazato, 2003; Drummond and Bapna, 2003; Watts et al., 2003; Lu et al., 2005; Xu X et al., 2006; Krämer et al., 2006), formation of secondary caries and bulk fracture remain challenges to the use of resins (Sarrett, 2005; Sakaguchi, 2005). Indeed, resin composites generally do not prevent secondary caries because they do not hinder bacteria colonization and plaque formation. In fact, several studies have indicated that resin composites have a greater accumulation of bacteria and plaque than other restorative materials (Svanberg et al., 1990; Imazato et al., 1994; Takahashi et al., 2004). Indeed, caries at the restoration margins are a frequent reason for replacing existing restorations (Mjör et al., 2000), accounting for 50-70% of all restorations (Deligeorgi et al., 2001; Frost, 2002).
Secondary caries may form in the tooth-restoration interface. Dental bonding systems are used to adhere resin composites to tooth structures (Spencer and Wang, 2002; Park et al., 2009; Pashley et al., 2011), but microleakage can allow bacteria to invade the interface. Residual bacteria can also exist in a clean tooth cavity prior to being packed with the resin composition.
Dental bonding systems that possess antibacterial properties could prove useful as an additional means of inhibiting the development of secondary caries by preventing the growth of residual and invading bacteria. Such antibacterial dental bonding systems would also find use in other applications to which dental bonding is employed, including dentin bonding, enamel bonding, tooth roots, marginal repair, as a crown cement, as an inlay/onlay cement, as a pit and fissure sealant, and as an orthodontic bracket adhesive or cement.